Nihon rinsho. Japanese journal of clinical medicine
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Bacterial factors stimulate the release of tissue factor as well as proinflammatory and antiinflammatory cytokines. TNF augments inflammation, TNF and IFN-gamma induce coagulation, and IL-1beta induces coagulation and fibrinolysis. IL-8 augments synergistic inflammation and coagulation. ⋯ Patients who died of SIRS/sepsis have been complicated with hypercoagulopathy and impaired fibrinolysis correlated with increased IL-10 production. Inhibition of IL-10 production or administration of fiblynolitic agents may be useful. Recently, activated protein C (APC) which has antiinflammatory effect has been paid attention in the treatment of SIRS/sepsis.
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It has been generally accepted that the frequency of the HLA-DR-antigen expression on monocytes reflects the individual's immune state; therefore it has been regarded as a key indicator of the immune status in SIRS (systemic inflammatory response syndrome)-sepsis. One of the diagnostic indices for the level of immunoparalysis, it characterizes CARS (compensatory anti-inflammatory response syndrome). Lately, it has been frequently reported that the frequency of HLA-DR-antigen expression on monocytes is abnormally reduced in those patients with SIRS-sepsis. Reports suggest that the prognosis is very poor in cases with long-term sharp declines in HLA-DR-antigen expression on monocytes.
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It is well known that various kinds of humoral mediators are discovered by the progress of a molecule biological method in recent years, and those humoral mediators that was produced excessively play an important role in the pathogenesis of SIRS and sepsis. However, it is impossible to measure those humoral mediators quickly in a present stage. The establishment of the fast measurement method of humoral mediators is indispensable for the judgment of septic conditions that change day by day. In this manuscript, we discussed that the role of humoral mediators in the SIRS and septic conditions and the clinical significance of established method for rapid measurement of humoral mediators.
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The activation of a pro-inflammatory cascade after infection, major surgery, burn or trauma appears to be important in the development of subsequent immune dysfunction, susceptibility to sepsis and multiple organ failure. It is well known that T-cell plays a critical role in the systemic response to infection. Distinct patterns of cytokines are produced by two different types of T-helper cells (Th). ⋯ We believe that severe sepsis clearly induce polarization of T-helper lymphocyte activity with a clear shift in Th2 direction. This type of response may lead immunosuppression. Modulation of Th cell subset predominance may present a novel therapeutic option in the treatment of severe sepsis.
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Recognition of pathogens by Toll-like receptors (TLRs) triggers innate immune responses via signaling pathways mediated by several Toll/IL-1R (TIR) domain-containing adaptors such as MyD88, TIRAP, and TRIF. MyD88 is a common adaptor that is essential for proinflammatory cytokine production, whereas TRIF mediates the MyD88-independent pathway from TLR3 and TLR4 that is responsible for type I interferon production in response to double-stranded RNA and LPS, respectively. TIRAP specifically participates in the MyD88-dependent pathways shared by TLR2 and TLR4, and TRAM is essential for the TLR4-mediated MyD88-independent pathway. Thus, TIR domain-containing adaptors play an important role in the TLR mediated signaling pathways.